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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were pretreated with various inducers of cytochrome P-450 before being exposed to pure normobaric oxygen (O2) in order to determine whether the inducers interfere with toxicity. The pulmonary and liver inducers beta-naphthoflavone (beta NF) and 3-methylcholanthrene (3MC) increased the survival rate and decreased the amount of pleural and lung fluid accumulation in adult rats exposed to oxygen. Phenobarbital (PB), which is essentially active in the hepatic microsomal cytochrome P-450, was less effective in counteracting oxygen toxicity. After 7 days of exposure to oxygen, none of the untreated rats survived, whereas 40, 73, and 90% survival was observed in rats treated with PB, 3MC, and beta NF, respectively. After 60 h of O2 exposure, significantly less pleural and lung fluid accumulation was observed in beta NF- and 3MC-treated rats than in untreated or PB-treated rats (p less than 0.001). Both beta NF and 3MC prevented the increase of lung peroxidation (assessed by measuring of malondialdehyde) and that of hydrogen peroxide production by lung microsomes induced by O2 exposure. These protective effects are associated with a large increase in the components of the pulmonary cytochrome P-450 system and its peroxidase activity and with an increased response to hyperoxia by lung antioxidant enzyme activities. In contrast, in control rats, the activities of the antioxidant enzymes were not increased, and both the quantity and the peroxidase activity of cytochrome P-450 were significantly decreased by O2 exposure. We conclude that in the rat, pretreatment by inducers of pulmonary cytochrome P-450 results in marked protection against O2 toxicity and an increase of antioxidant enzyme response to hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection of rat from oxygen toxicity by inducers of cytochrome P-450 system. 283 Aug 13

Daily exposures of rabbits to the HBO (2 ata, 1 hr) enhanced activity of glutathione-peroxidase for all 28 days of exposure. Other parameters of the antioxidative defence and the contractile function remained unchanged. The 2.5-ata oxygenation sharply reduced the activity of antioxidative enzymes, the antioxidative activity of lipids, and the tissue resistance against the induced peroxide oxidation of lipids. The heart contractile function was obviously worsened. Sites of necrosis appeared in the myocardium tissue. Increase in oxygenation seems to lead to changes of adaptation of the antioxidative system, but the exhaustion of the latter's power reserves potentiates the toxic effect of hyperoxia.
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PMID:[Contractile function and antioxidative system of the myocardium of the intact rabbit during hyperbaric oxygenation]. 301 94

1. Various parameters related to oxidative stress were measured in adult Discoglossus pictus acclimated for 15 days to either normoxia or hyperoxia (PO2 = 710 mmHg). 2. Total weight of the toads and total and relative wet weight of liver, kidneys, lungs and heart were not changed by hyperoxic acclimation. 3. In vivo tissue peroxidation increased in lung, decreased in skeletal muscle, and was not changed in liver, kidney, heart and skin after hyperoxic exposure. 4. Hyperoxic acclimation increased catalase activities in the lung, liver, kidney and heart but not in skeletal muscle and skin. 5. Liver showed higher GSH-peroxidase activity with cumene-OOH than with H2O2 as substrate, whereas lung, skeletal muscle and skin presented similar GSH-peroxidase activities with both substrates. 6. GSH-peroxidase activities did not change between hyperoxic and normoxic animals in liver, lung, skeletal muscle and skin. 7. These results show that catalase, not GSH-peroxidase, is the principal H2O2 detoxifying enzyme involved in the adaptation of D. pictus to hyperoxia.
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PMID:Physiological significance of catalase and glutathione peroxidases, and in vivo peroxidation, in selected tissues of the toad Discoglossus pictus (Amphibia) during acclimation to normobaric hyperoxia. 324 21

Mice were given i.v. injections of various tumor cell lines and, beginning 24 h later exposed for 3 weeks to 70% oxygen. Hyperoxia reduced the number of lung colonies derived from MT-7 cells (originally a mammary carcinoma) and of the lung-tumor derived cell lines 498 and Line-1 early passage. Lung colonies derived from Line-1 late passage, lines M109, B16-F10 and Lewis lung carcinoma were oxygen resistant. Lung metastases following i.m. injection of MT-7 cells were oxygen-sensitive and metastases derived from B16-F10 cells or Lewis lung carcinoma were oxygen resistant. Pre-exposure of mice for 48 h to 100% oxygen enhanced colony formation for all cell lines examined whereas exposure to 100% oxygen after i.v. injection only curtailed the growth of the cell lines previously shown to be sensitive to 70% oxygen. There was no correlation between oxygen sensitivity or resistance and the levels of total glutathione or activities of superoxide dismutase (SOD), glutathione reductase or peroxidase or glucose 6-phosphate dehydrogenase in the cell lines. However, upon injection in mice a resistant cell line increased its anti-oxidant defense mechanisms while growing in vivo whereas a sensitive cell line failed to show such adaptation.
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PMID:Effects of hyperoxia on growth of experimental lung metastasis. 334 81

Administration of monoamine oxidase type A inhibitor clorgyline to rats before hyperoxia prevented oxygen-induced increase in diene conjugate and Shiff's base brain and plasma levels in hyperoxia. This was due to antioxidative effect of clorgyline which resulted in stabilization of blood cellular membranes. Clorgyline had a normalizing effect on extraerythrocyte hemoglobin level, total peroxidase activity and glucose-6-phosphate dehydrogenase activity in the serum.
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PMID:[Effect of clorgyline on the intensity of lipid peroxidation and on erythrocyte membrane stability in hyperoxia]. 380 52

Different regimens of oxygenation were studied in rats: acute hypoxia (9,000 m, 3 hrs), acute hyperoxia (0.7 MPa O2), which caused convulsions, and their simultaneous effects. Under these conditions the following parameters were evaluated: the rate of Fe(2+)-induced chemiluminescence, content of nitrogen and peptide catabolism products (urea, urates and middle molecule peptides) as well as total peroxidase activity, content of extraerythrocyte hemoglobin and lactic acid in blood plasma. Distinct inhibition of the chemiluminescence rate was found in all the three experimental groups studied; accumulation of uric acid, middle mass peptides, extraerythrocyte hemoglobin, lactic acid as well as an increase in the total peroxidase activity were observed in hyperoxia and in simultaneous effect of hypo- and hyperoxia; total peroxidase activity was decreased in rats with acute hypoxia. Accumulation of urates and middle mass peptides was considered according to these substances capacity to inhibit free radical oxidation in vivo.
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PMID:[Chemiluminescent analysis and some indicators of nitrogen catabolism in rat blood plasma in hypoxia with subsequent hyperoxia]. 797 75

The role of the emoxipin (Em.) (2-ethyl-6-methyl-3-oxipyridine) in the correction of the free radical oxidation and allied processes in lung tissues and blood plasma under high-pressure oxygen-prolonged action has been investigated. The studied oxygen exposure (0.3 MPa, 5h) causes the lung stage of oxygen intoxication. It is confirmed by exterior morphological assessment of the lung. The lipid peroxidation increase in lung tissue and blood plasma as well as erythrocyte membranes destabilization result from oxygen exposure. Lipid peroxidation intensity was estimated by determining of content of lipid peroxidation molecular products such as diene conjugates and Shiffs' bases. Erythrocyte membranes stability was evaluated with hemoglobin yield, total iron level and total peroxidase activity in blood plasma. Emoxipin was injected intraperitoneally in a dose 150 mg per 1 kg rats' weight just before the oxygen exposure. Emoxipin is found to improve physiological state of animals and to increase their survival; it normalizes morphology of the lungs and their state; stabilizes erythrocyte membranes injured under oxygen exposure; decreases intensity of lipid peroxidation processes in the lungs and in blood plasma which was previously increased under hyperoxia.
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PMID:[Emoxipin correction of disorders of lipid peroxidation as affected by a slight excess of oxygen pressure]. 799 32

Age peculiarities of functioning of antioxidizing system of chickens in postnatal ontogenesis were exposed for the first time. High superoxide dismutase activity in the organs and tissues of the 24 hours' chickens is to be considered as a compensatory defense during the transition from hypoxia of the end of embryo development to the relative hyperoxia after hatching. In the early postnatal ontogenesis superoxide dismutase activity declines, while the activity of peroxidase, catalase and enzymes of glutathione cycle increases. The mentioned changes reach maximum at the age of 20-30 days. The insufficient defense of chicken organism from the active forms of oxygen leads to the shift of oxidizing processes towards free-radical ones, to the decrease of concentration of lipids, phospholipids, retinol, inhibition of protein biosynthesis. Intensification of the processes of lipids peroxidation occurs before the decrease of alpha-tocopherol level. Functional dependence of chickens growth intensity on biochemical indices of their antioxidant system is of complex nonlinear character and is described by the forth degree polynomials.
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PMID:[The antioxidant system and lipid peroxidation in chickens during postnatal ontogenesis]. 859 91

Alveolar epithelial injury occurs universally in common respiratory illnesses associated with diffuse lung damage. After alveolar injury, type II cells proliferate and reestablish epithelial integrity, thereby restoring normal lung structure and function. However, the regulation of type II cell proliferation and alveolar epithelial repair is poorly understood. Hepatocyte growth factor/scatter factor (HGF/SF) is a heparin-binding growth factor that has been shown to be mitogenic for cultured alveolar type II cells. In this study, we determined the effect of intratracheal instillation of rhHGF/SF on type II cell proliferation in vivo. To quantify the alveolar type II cell proliferative response, we developed a double-label immunohistochemical technique to detect replicating alveolar type II cells in formalin-fixed lung sections that utilized the identification of proliferating cells by bromodeoxyuridine (BrdUrd) incorporation into DNA and alveolar type II cells by 3F9 immunoreactivity. BrdUrd detection was optimized by enzymatic antigen recovery and silver intensification of the horseradish peroxidase reaction product. Intratracheal instillation of rhHGF/SF induced a time- and dose-dependent increase in type II cell proliferation. The type II cell labeling index increased to 12.3 +/- 6.0% 48 h after 1.0 mg/kg rhHGF/SF administration, compared with 2.6 +/- 0.9% after PBS instillation. To compare the normal type II cell reparative response with the level of proliferation after exogenous rhHGF/SF administration, we measured the specific alveolar type II cell labeling index in rat lung sections obtained from animals exposed to hyperoxia for 50 h and then allowed to recover in room air. After 1 day of recovery, the alveolar type II cell labeling index was 0.45 +/- 0.2%. The specific labeling index increased to 5.4 +/- 1.3% at 2 days and then declined to 0.31 +/- 0.16% 5 days after hyperoxia exposure. In animals not exposed to hyperoxia, the alveolar type II cell labeling index was 0.6 +/- 0.14%. These studies demonstrated that intratracheal instillation of rhHGF/SF promoted alveolar type II cell proliferation in vivo. The maximal level of type II cell proliferation after rhHGF/SF administration was more than twice that reached during recovery from hyperoxia exposure. Thus, intratracheal instillation of HGF/SF may provide a potential strategy to promote type II cell proliferation and augment alveolar epithelial repair after lung injury.
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PMID:Intratracheal administration of hepatocyte growth factor/scatter factor stimulates rat alveolar type II cell proliferation in vivo. 891 64

It is well established that the phenotype of the pulmonary vascular surface can be affected by injurious stimuli, but the few proteins for which the expression and/or activity have been studied make up only a small fraction of the entire spectrum of luminal cell membrane proteins. To expand the capability for studying such proteins, we developed a method for biotinylating cell membrane proteins accessible via the vascular lumen in the isolated-perfused rat lung and examined the impact of hyperoxia on the spectrum of the biotinylated proteins. Labeling was carried out either by single-pass bolus injection of the cell impermeant biotinylation reagent sulfosuccinimidyl 6-biotin-amido hexanoate (NHS-LC-biotin) into the pulmonary artery cannula or by the addition of NHS-LC-biotin to a lung homogenate. Lung membrane fractions were prepared, and the proteins were separated by SDS-polyacrylamide gel electrophoresis and transferred to nitrocellulose by electroblotting. The biotinylated proteins were visualized using a chemiluminescent substrate for streptavidin-linked horseradish peroxidase. The spectrum of proteins biotinylated via the vasculature was distinct from that of the biotinylated lung homogenate. Lectin affinity purification of biotinylated proteins from the lung membrane fractions of normal lungs biotinylated via the vasculature revealed characteristic spectra that were reproducibly different from those from rats exposed to hyperoxia for 48-60 h. These results demonstrate that biotinylation of membrane proteins accessible to an extracellular reagent during a single transit through the pulmonary vascular bed is feasible and that the spectrum of these labeled proteins reveals the effects of hyperoxic lung injury. The affinity of biotin for streptavidin makes this procedure potentially useful as a means of separating the labeled membrane proteins from the much larger population of membrane proteins that are not accessible via the vasculature, e.g., intracellular membrane proteins and plasma membrane proteins of cell types in luminally inaccessible regions of the intact lung. The consistent changes in the spectrum of labeled proteins seen with hyperoxia suggest that in itself the spectrum may be a useful encryption of certain aspects of vascular pathophysiology.
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PMID:Biotinylation of membrane proteins accessible via the pulmonary circulation in normal and hyperoxic rats. 912 3


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